Key result
Evolutionary analysis of kinetoplastid myosin genes reveals expansion through duplication, loss, and potential neofunctionalization.
Why the study?
The classification and evolutionary history of myosin genes in trypanosomatids and related species were unclear, including the status of orphan myosins and gene diversification.
The study reclassifies previously 'orphan' myosins in trypanosomatids into a new class (XXXVI) and demonstrates their evolutionary history of expansion, loss, and neofunctionalization.
No immediate clinical implications for kinetoplastid infections; leaves open functional validation of myosin class XXXVI as a research target.
Myosins are motor proteins that comprise a large and diversified family important for a broad range of functions. Two myosin classes, I and XIII, were previously assigned in Trypanosomatids, based mainly on the studies of Trypanosoma cruzi, T. brucei and Leishmania major, and important human pathogenic species; seven orphan myosins were identified in T. cruzi. Our results show that the great variety of T. cruzi myosins is also present in some closely related species and in Bodo saltans, a member of an early divergent branch of Kinetoplastida. Therefore, these myosins should no longer be considered "orphans". We proposed the classification of a kinetoplastid-specific myosin group into a new class, XXXVI. Moreover, our phylogenetic data suggest that a great repertoire of myosin genes was present in the last common ancestor of trypanosomatids and B. saltans, mainly resulting from several gene duplications. These genes have since been predominantly maintained in synteny in some species, and secondary losses explain the current distribution. We also found two interesting genes that were clearly derived from myosin genes, demonstrating that possible redundant or useless genes, instead of simply being lost, can serve as raw material for the evolution of new genes and functions.
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Souza et al. (2018) studied Trypanosomatid parasites. Evolutionary analysis of myosin genes was evaluated. Evolutionary analyses of kinetoplastid myosin genes revealed a history of expansion through gene duplication, secondary losses, and potential neofunctionalization.
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